From Peripheral to Central: The Role of ERK Signaling Pathway in Acupuncture Analgesia Public Deposited

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Creator
  • Park, Ji-Yeun
  • Park, Jongbae J.
  • Jeon, Songhee
  • Doo, Ah-Reum
  • Kim, Seung-Nam
  • Lee, Hyangsook
  • Chae, Younbyoung
  • Maixner, William
  • Lee, Hyejung
  • Park, Hi-Joon
Abstract
  • Despite accumulating evidence of the clinical effectiveness of acupuncture, its mechanism remains largely unclear. We assume that molecular signaling around the acupuncture needled area is essential for initiating the effect of acupuncture. To determine possible bio-candidates involved in the mechanisms of acupuncture and investigate the role of such bio-candidates in the analgesic effects of acupuncture, we conducted 2 stepwise experiments. First, a genome-wide microarray of the isolated skin layer at the GB34-equivalent acupoint of C57BL/6 mice 1 hour after acupuncture found that a total of 236 genes had changed and that extracellular signal–regulated kinase (ERK) activation was the most prominent bio-candidate. Second, in mouse pain models using formalin and complete Freund adjuvant, we found that acupuncture attenuated the nociceptive behavior and the mechanical allodynia; these effects were blocked when ERK cascade was interrupted by the mitogen-activated protein kinase kinase (MEK)/mitogen-activated protein kinase (MAPK) inhibitor U0126 (.8 μg/μL). Based on these results, we suggest that ERK phosphorylation following acupuncture needling is a biochemical hallmark initiating the effect of acupuncture including analgesia.
Date of publication
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DOI
Identifier
Resource type
  • Article
Rights statement
  • In Copyright
Journal title
  • The Journal of Pain
Journal volume
  • 15
Journal issue
  • 5
Page start
  • 535
Page end
  • 549
Language
  • English
ISSN
  • 1528-8447
  • 1526-5900
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